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肿瘤细胞中磷脂酰肌醇3激酶(phosphatidylinositol 3-kinase,PI3K)/蛋白激酶B(protein kinase B,PKB,又称Akt)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,m TOR)信号通路高度激活,该通路与肿瘤细胞增殖、分化、凋亡、黏附、迁移和代谢等过程密切相关。小分子抑制剂NVP-BEZ235作为双蛋白激酶抑制剂,可同时靶向PI3K和m TOR通路。近年来的多项研究证实,NVP-BEZ235通过多种机制对20多种人类肿瘤细胞和动物模型发挥高效的抗肿瘤作用。本文主要综述NVP-BEZ235通过影响肿瘤细胞的增殖、细胞周期、凋亡、自噬、分化、血管生成和上皮间质转化(epithelial-mesenchymal transition,EMT)等而发挥抗肿瘤效应。
Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, also known as Akt)/mammalian target of rapamycin (m TOR) in tumor cells The signaling pathway is highly activated, and the pathway is closely related to the proliferation, differentiation, apoptosis, adhesion, migration and metabolism of tumor cells. The small molecule inhibitor NVP-BEZ235 acts as a dual protein kinase inhibitor and can simultaneously target the PI3K and mTOR pathways. A number of studies in recent years have confirmed that NVP-BEZ235 exerts highly effective anti-tumor effects on more than 20 human tumor cells and animal models through various mechanisms. In this review, we reviewed the effects of NVP-BEZ235 on tumor cell proliferation, cell cycle, apoptosis, autophagy, differentiation, angiogenesis, and epithelial-mesenchymal transition (EMT).